What's Hot
What's Hot
News flashes are posted here frequently to keep you up-to-date with the latest advances in health and longevity. We have an unparalleled track record of breaking stories about life extension advances.
Vitamin D supplementation helps relieve chronic back pain
January 30 2017. A clinical trial reported in the January 2017 issue of Pain Physician uncovered a benefit for supplementing with vitamin D among individuals with chronic lower back pain. The condition is the second most common pain complaint after headache and can be notoriously resistant to treatment.
The trial included 68 men and women who had chronic lower back pain for at least three months that did not respond to medications and physical therapy. Subjects were limited to those with plasma 25-hydroxyvitamin D3 levels measured at the beginning of the trial of less than 30 nanograms per milliliter (ng/mL). Participants received 60,000 international units (IU) vitamin D3 given orally once per week for eight weeks. Pain and disability were scored at the beginning of the study and at two, three and six months.
Ninety percent of the subjects had deficient levels of 20 ng/mL or lower and 10% had insufficient levels of greater than 20 ng/mL to 29 ng/mL at the beginning of the trial. Following supplementation, 66% of the patients attained sufficient levels of more than 29 ng/mL. Pain and disability scores significantly improved at two, three and six months in comparison with scores obtained at the study’s onset.
In their discussion of the findings, authors Babita Ghai, MD, DNB and colleagues observe that vitamin D exerts anatomic, hormonal, neurologic and immunologic influences on pain expression. “Our findings provide a reasonable explanation and justification for advising dietary supplementation as well as therapeutic medication to achieve normal vitamin-D levels in patients with musculoskeletal pain,” they write. “It is advisable to get adequate sunlight exposure as well as vitamin D and calcium supplementation along with physical exercise to mitigate the morbidity induced by the disability caused by abnormal vitamin D homeostasis.”
—D Dye
Metformin disrupts head and neck tumor growth
January 27 2017. On January 25, 2017, The Laryngoscope reported the discovery of researchers at Thomas Jefferson University of mechanisms associated with the drug metformin against cancer of the head and neck.
"This study is the first step in showing how metformin acts on head and neck tumors, and we are excited that it could eventually offer patients a method of improving their outcomes with few side effects," announced senior author Ubaldo Martinez-Outschoorn.
Acting on the knowledge of improved head and neck cancer outcomes among metformin-treated diabetic patients in comparison with nondiabetics, Dr Martinez-Outschoorn and colleagues examined tumor cells derived from 39 nondiabetic cancer patients before and after they were treated with metformin. The subjects were given metformin doses that were approximately half of those commonly received by diabetics. The team found an increase in tumor cell apoptosis (programmed cell death) as well as signs of deterioration of cancer-supporting fibroblasts surrounding the tumor cells, suggesting that these cells were less able to assist their neighboring cancer cells’ growth and metastasis.
"Because tumors need a lot of energy to grow quickly, throwing a wrench in their energy-production pathway makes this kind of cancer more susceptible to standard therapies," explained first author Joseph Curry, MD.
"This study demonstrates that metformin has effects on head-and-neck cancers, at safe doses, that are at or lower than what is given to diabetic patients and that it changes head-and-neck tumor biology in a way that likely makes the cancer easier to kill," concluded coauthor Madalina Tuluc, MD, PhD. "Metformin disrupts the cancer's most efficient method of generating fuel for its growth and shuts off the cancer's support system."
"The next step would be to test these doses of metformin in phase II clinical trials with a greater number of patients," Dr Martinez-Outschoorn added.
—D Dye
Metabolic syndrome increases the need for vitamin E
January 25 2017. An article appearing on January 11, 2017 in the American Journal of Clinical Nutrition provides more evidence for a higher vitamin E requirement among people with metabolic syndrome, a cluster of factors that increase the risk of diabetes and cardiovascular disease. The research builds on findings reported in the November 2015 issue of the journal, in which Richard S. Bruno and colleagues had determined that vitamin E was less bioavailable in subjects with metabolic syndrome than healthy subjects.
In the current double-blind, crossover trial, Dr Bruno and his associates measured two breakdown products of deuterium-labeled vitamin E consumed by ten healthy adults and ten who had metabolic syndrome. They found those with metabolic syndrome eliminated less of the vitamin than the healthy subjects, indicating increased need, however, conventional blood tests showed levels that were similar to those of the healthy group.
“The research showed that people with metabolic syndrome need about 30-50 percent more vitamin E than those who are generally healthy,” reported lead author Maret Traber of the Linus Pauling Institute. “We’ve discovered that vitamin E levels often look normal in the blood, because this micronutrient is attracted to high cholesterol and fat. So vitamin E can stay at higher levels in the circulatory system and give the illusion of adequate levels, even as tissues are deficient. This basically means that conventional vitamin E blood tests as they are now being done are useless.”
“In previous work we showed that people with metabolic syndrome had lower bioavailability of vitamin E,” she noted. “Our current work uses a novel approach to measure how much vitamin E the body needs. This study clearly demonstrates that people with metabolic syndrome need a higher intake of this vitamin.”
—D Dye
Supplementation with vitamin D associated with improved testosterone, erectile function among middle-aged men
January 23 2017. A study reported on January 11, 2017 in The Aging Male found improvements in testosterone levels, erectile function and indicators of metabolic syndrome among men who received vitamin D over a one year period. “Given that patients with low total testosterone often have low vitamin D levels, collectively, research suggests a relationship between low vitamin D and low total testosterone, and increased risk of type 2 diabetes mellitus,” note Ondor Canguven of Hamad General Hospital in Doha, Qatar and colleagues.
The study included 102 men between the ages of 35 to 65 with vitamin D levels of less than 30 nanograms per milliliter (ng/mL). Upon enrollment and 3, 6, 9 and 12 months, blood samples were analyzed for serum total testosterone, estradiol, hemoglobin A1c, lipids, 25-hydroxyvitamin D and other factors, and questionnaires were administered to assess erectile function. Participants received 600,000 international units (IU) of vitamin D in an orally administered solution at the beginning of the study and monthly thereafter until a serum level of 30 ng/mL was attained, after which the dose was given every other month.
Serum vitamin D and total testosterone significantly increased with each measurement over the course of the study. This was accompanied by an improvement in erectile function scores and decreases in estradiol, parathyroid hormone, hemoglobin A1c, low-density lipoprotein (LDL) cholesterol, triglycerides, and body mass index.
As potential mechanisms for vitamin D in erectile function, Dr Canguven and associates suggest improved endothelial integrity, increased nitric oxide mediated vascular dilation, and more.
“This study demonstrated that, in middle-aged vitamin D-deficient men, vitamin D treatment improves sexual hormones, metabolic syndrome and erectile dysfunction,” the authors conclude.
—D Dye
Research validates inflammaging theory
January 20 2017. Inflammaging, defined as chronic, systemic low-grade inflammation that occurs with aging in the absence of overt infection, has been hypothesized as a mechanism of age-associated disease and premature mortality. A cause of inflammaging has been attributed to lifetime exposure to a variety of antigens via the intestine.
In an article published on January 3, 2017 in Scientific Reports, Korean researchers report the finding in mice of an age-related decrease in supportive pericytes that surround the intestinal blood vessels’ endothelial cells, which increases vascular leakage. This phenomenon was ascribed to upregulation of angiopoetin-2 in the microvascular endothelial cells due to the inflammatory cytokine tumor necrosis factor-alpha (TNF-a) that originates from a type of macrophage (white blood cells that consume foreign antigens and other undesirable material).
“A hallmark of age-associated chronic inflammation would be macrophage infiltration,” the authors explain. “In intestine, the epithelial lining separates internal organs from the enteric environment loaded with various foreign substances including microbiota and its metabolic products as well as nutrients and wastes.”
“Antigenic burdens encountered in intestine throughout life create the condition of chronic stage of inflammation, which accumulates M2-like macrophages expressing TNF-α,” they write. “The TNF-α induces vascular leakage to facilitate recruitment of immune cells into intestine under the chronic inflammatory setting.”
"This study is significant as we have newly identified the mechanisms of aging associated with inflammation increase and opened possibilities of applied researches on aging delay through inflammation control as well as anti-aging,” commented lead researcher Sang Chul Park. “We will conduct follow-up studies to find ways to extend human healthy life by controlling inflammatory cells and vascular leakage to delay aging."
—D Dye
More evidence for calorie restriction’s longevity effect
January 18 2017. An article published on January 17, 2017 in Nature Communications reports the conclusion of researchers at the University of Wisconsin-Madison and the National Institute on Aging (NIA) that calorie restriction among older rhesus monkeys results in longer life. The research, which attempted to resolve conflicting findings concerning the effect of calorie restriction on life span, is the first collaboration between the two competing research teams.
In 2009, researchers at the University of Wisconsin-Madison reported less disease and longer survival in monkeys given calorie restricted diets compared with those whose eating was unrestricted. However, in 2012, the NIA conducted a similar study that failed to uncover a survival benefit. "These conflicting outcomes had cast a shadow of doubt on the translatability of the caloric-restriction paradigm as a means to understand aging and what creates age-related disease vulnerability," commented Rozalyn Anderson, who is one of the current report's authors.
Comparison of the studies, which included data from close to 200 monkeys, revealed that the animals had their diets restricted at different ages. (Eating less is more beneficial to adult and older primates than younger animals.) The Wisconsin group’s control monkeys that started their diets at an older age ate more than NIA control monkeys, and diet composition was different between the research facilities. It was additionally found that female monkeys were less vulnerable to adiposity’s adverse effects.
“The NIA and UW nonhuman primate ageing and calorie studies address a central concept of relevance to human ageing and human health: that the age-related increase in disease vulnerability in primates is malleable and that ageing itself presents a reasonable target for intervention,” the authors write.
“Taken together these data confirm that health benefits of calorie restriction are conserved in monkeys and suggest that calorie restriction mechanisms are likely translatable to human health,” they conclude.
—D Dye
Insect queens’ longer life associated with lower markers of oxidative damage
January 16 2017. A study of termites adds more evidence to the free radical theory of aging submitted by Denham Harman, MD, in the 1950s. Researchers in Japan have uncovered a correlation between the longer lifespan of termite queens and a decrease in oxidative damage in comparison with shorter-lived worker and soldier insects. While long life is usually accompanied by the trade-off of diminished fertility, the opposite is true for termite queens that produce most or all of the offspring in a colony. The study was reported on January 11, 2017 in PLOS ONE.
Eisuke Tasaki of Tottori and Yamaguchi Universities and colleagues measured markers of oxidative damage in DNA, proteins and lipids, as well as the expression of antioxidant enzyme genes in queen and worker termites. They found significantly lower levels of the marker of DNA oxidative damage 8-hydroxy-2’-deoxyguanosine following ultraviolet (UV) irradiation exposure in queens compared to worker termites. Protein carbonyls, which are biomarkers of oxidative damage to protein, and levels of malondialdehyde, a marker of lipid peroxidation, were significantly lower in queens than workers in normal conditions as well as after UV irradiation.
Queen termites had two times as much activity of the antioxidant enzyme catalase and seven times more expression of the catalase gene RsCAT1 compared to workers. Queens also had greater activity of the antioxidant enzyme peroxiredoxin.
“These results suggested that this efficient antioxidant system can partly explain why termite queens achieve long life,” the authors conclude. “To the best of our knowledge, we have revealed for the first time that termite queens suffer lower levels of oxidative damage than non-reproductive workers, and that an efficient antioxidant system consisting of several antioxidant enzymes, especially high catalase activity from RsCAT1 gene expression, may play an important role in their oxidative stress resistance.”
—D Dye
Niacin could help with early onset Parkinson’s disease
January 13 2017. A study reported on December 23, 2016 in Biology Open suggests a benefit for niacin (vitamin B3) in the treatment of early stage Parkinson’s disease.
The research involved fruit flies with a mutation which results in a condition similar to human Parkinson’s disease. L. Miguel Martins and colleagues at the University of Leicester fed the flies a diet supplemented with niacin, which is a precursor to nicotinamide adenine dinucleotide (NAD), a coenzyme needed for the generation of energy in the cells’ mitochondria. NAD also helps protect neurons from degeneration.
"Parkinson's disease occurs when dopaminergic neurons in a part of the brain called the substantia nigra are lost,” Dr Martins explained. “This can happen for a variety of reasons, but in some hereditary cases, the main problem is unhealthy mitochondria - the organelles that power the cell.”
“Mutations in genes such as PINK1 prevent cells from clearing out the defective powerhouses,” he continued. “When they accumulate, neurons can't get enough energy and die. The faulty mitochondria also release toxic molecules that damage their genes encoded by DNA.”
"Curiously enough, there's a compound in the body that's important for both energy generation and DNA repair,” Dr Martins noted. ”It's called NAD. With all the mitochondrial damage going on, we wondered if in cases of Parkinson's the molecule ends up in short supply."
Flies with the PINK1 mutation that received niacin had fewer faulty mitochondria and less neuron loss compared to those that did not receive the vitamin. Blocking DNA repair from depleting NAD resulted in healthier mitochondria and greater neuron survival, as well as longer lifespan.
"This study strengthens the therapeutic potential for vitamin B3/niacin-based dietary interventions in the treatment of Parkinson's disease" Dr Martins concluded. "The results suggest that in familial Parkinson's, available NAD is critical for keeping mitochondria in shape and the disease at bay. Drugs that block NAD-consuming DNA repair already exist to treat cancer. Loading up on niacin probably can't hurt either.”
—D Dye
Mediterranean plants could prolong life in neurodegenerative disease
January 11 2017. The January 18, 2017 issue of Neuroscience Letters reports the discovery of researchers at the University of Malta and the University of Bordeaux of a life-extending effect for two plants found in the Mediterranean region.
Ruben J. Cauchi, PhD, and colleagues investigated the properties of brown seaweed and prickly pear in fruit fly models of Alzheimer’s disease and Parkinson’s disease. The diseases are characterized by the accumulation of sticky proteins that cause damage to the nervous system. “We have long been screening plants scattered across the Mediterranean for small molecules that interfere with the build-up of toxic protein aggregates,” commented study co-author Neville Vassallo, MD, PhD. “The robust effects of chemicals derived from the prickly pear and brown seaweed confirm that our search has certainly not been in vain.”
Initial testing of either plant extract resulted in greater viability in yeast that expressed a genetic variant causing the accumulation of amyloid beta, which is elevated in Alzheimer’s disease. In fruit flies that were genetically modified to develop Alzheimer’s disease symptoms, the administration of seaweed extract prolonged median life span by two days and prickly pear extract was associated with a four day extension. (One day in fruit flies’ lives is equivalent to a year of human life.) Survival also improved in treated flies bred to express increased alpha-synuclein, a protein that accumulates in Parkinson’s disease.
“We believe that the discovery of bioactive agents that target pathways that are hit by multiple neurodegenerative conditions is the most viable approach in our current fight against brain disorders,” Dr Cauchi stated. “A clear advantage of the drugs used in this study is that, in view of their excellent safety profile, they are already on the market as nutraceuticals and cosmeceuticals.”
—D Dye
Mediterranean diet associated with increased brain volume retention
January 09 2017. An article published online on January 4, 2017 in the journal Neurology® reports an association between adherence to a Mediterranean-type diet and greater retention of brain volume among older individuals over a three year period.
A Mediterranean diet, which is characterized by an abundance of fruit, vegetables, olive oil, beans and grains, and moderate amounts of fish and dairy products, has been linked with less inflammation, improved cognitive function, a lower risk of Alzheimer’s and Parkinson’s disease, and decreased mortality from cancer and cardiovascular disease.
The study included 401 dementia-free residents of Scotland who were approximately 70 years of age upon enrollment. Dietary questionnaire responses were scored according to Mediterranean diet adherence. Magnetic resonance imaging conducted at the ages of 73 and 76 years assessed overall and gray matter volume, as well as cortical thickness.
The researchers observed an association between lower adherence to the Mediterranean diet and a greater reduction in total brain volume over three years. The difference in diet explained 0.5% of total brain volume variation, compared to 1% variation due to normal aging. In contrast with the findings of previous research, fish and meat consumption did not show an association with brain changes.
"As we age, the brain shrinks and we lose brain cells which can affect learning and memory," stated first author Michelle Luciano, PhD, of the University of Edinburgh. "This study adds to the body of evidence that suggests the Mediterranean diet has a positive impact on brain health."
"In our study, eating habits were measured before brain volume was, which suggests that the diet may be able to provide long-term protection to the brain," she added. "Still, larger studies are needed to confirm these results."
—D Dye
Grilled and smoked meat consumption associated with greater mortality risk in breast cancer survivors over 17.6 year median follow-up period
January 06 2017. A study reported in the JNCI: Journal of the National Cancer Institute found a greater risk of dying over a median 17.6 years of follow-up among female breast cancer survivors who had a higher intake of grilled, barbecued, and smoked meat in comparison with those who consumed lower amounts.
The current study included 1,508 women diagnosed with breast cancer. Interviews conducted during 1996-1997 and five years later obtained information concerning the intake of grilled, barbequed and smoked meat.
Five hundred ninety-seven deaths occurred during a median 17.6 year period, including 237 deaths associated with breast cancer. In comparison with an intake below the median, having a higher intake of the meats prior to diagnosis was associated with a 23% greater risk of dying from any cause. For women who continued to consume higher amounts of grilled, barbecued and smoked meat after diagnosis, the risk of all-cause mortality was 31% higher than those whose intake was lower.
Meat cooked at high temperatures contains polycyclic aromatic hydrocarbons (PAHs) and other compounds associated with breast cancer risk. The study is the first to examine whether the intake of this source of PAH influences survival in women diagnosed with breast cancer.
“High intake of grilled/barbecued and smoked meat may increase mortality after breast cancer may increase the mortality risk among breast cancer survivors,” authors Humberto Parada, Jr, MPH, of the University of North Carolina Chapel Hill and colleagues conclude.
—D Dye
PQQ supplementation associated with protection against fatty liver
January 04 2017. On December 22, 2016, the Journal of the Federation of American Societies for Experimental Biology (FASEB Journal) reported the results of an experiment that found an association between the intake of pyrroloquinoline quinone (PQQ) in obese mice and a lower risk of the development of nonalcoholic fatty liver disease (NAFLD) in their offspring.
"We know that infants born to mothers with obesity have a greater chance of developing NAFLD over their lifetime, and in fact one-third of obese children under 18 may have undiagnosed fatty liver disease that, when discovered, is more likely to be advanced at the time of diagnosis," stated lead author Karen Jonscher, PhD, of the University of Colorado Anschutz Medical Campus. "The goal of our study, which we carried out using a mouse model of obese pregnancy, was to determine whether a novel antioxidant given to mothers during pregnancy and breastfeeding could prevent the development of NAFLD in the offspring."
Dr Jonscher and colleagues fed female mice a healthy diet or a Western-style diet that contained a high amount of fat and sugar. Some of the animals in both groups received drinking water enhanced with PQQ. Mice born to the animals were kept on the diets for 20 weeks. While offspring that received a Western diet experienced greater weight gain, the addition of PQQ was associated with less fat and inflammation in the liver.
"Pyrroloquinoline quinone, or PQQ, is a natural antioxidant found in soil and many foods and enriched in human breast milk," Dr Jonscher noted. "Perhaps supplementing the diet of obese pregnant mothers with PQQ, which has proven safe in several human studies, will be a therapeutic target worthy of more study in the battle to reduce the risk of NAFLD in babies.”
—D Dye
AMA journal associates iron deficiency with hearing loss
January 02 2017. An article published online on December 29, 2016 in JAMA Otolaryngology-Head & Neck Surgeryreports an association between iron deficiency anemia and hearing loss.
Kathleen M. Schieffer, BS, of Pennsylvania State University College of Medicine and colleagues evaluated data from 305,339 men and women between the ages of 21 and 90 years who visited Penn State Hershey Medical Center during 2011-2015 and had information available concerning serum ferritin and hemoglobin levels. Low serum ferritin levels were defined as less than 12.0 nanograms per milliliter and low hemoglobin levels were determined according to age and sex.
Hearing loss identified during past visits was categorized as conductive (associated with the bones of the middle ear), sensorineural, or combined loss (conductive and/or sensorineural loss, deafness or loss due to unspecified causes). Subjects who had iron deficiency anemia had 82% higher odds of being diagnosed with sensorineural hearing loss and a greater than two-fold increased risk of combined hearing loss.
While too much iron is undesirable for many reasons, deficient levels are also associated with potentially severe adverse conditions. The authors note that only one artery supplies blood to the cochlea of the ear, and that low hemoglobin levels that impair the blood’s oxygen carrying capacity can lead to ischemia in this area.
“Iron deficiency anemia is easily treated with several months of oral iron supplementation,” Dr Schieffer and colleagues observe. “Iron deficiency anemia is associated with a large number of related morbidities (eg, fatigue and reduced work capacity), which are also likely to improve with treatment. Additional studies are needed to determine whether there is a link between iron supplementation and hearing status.”
—D Dye
